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  • 1
    Online Resource
    Online Resource
    The Signaling Pathways Involved in the Antiatherosclerotic Effects Produced by Chinese Herbal Medicines
    Hindawi Limited ; 2018
    In:  BioMed Research International Vol. 2018 ( 2018-06-13), p. 1-16
    Details
    In: BioMed Research International, Hindawi Limited, Vol. 2018 ( 2018-06-13), p. 1-16
    Abstract: Cardiovascular diseases (CVDs) are considered to be the predominant cause of death in the world. Chinese herb medicines (CHMs) have been widely used for the treatment of CVDs in Asian countries for thousands of years. One reason of high efficacy of CHMs in treating CVDs is attributed to their inhibition in atherosclerosis (AS) development, a critical contributor to CVDs occurrence. Cumulative studies have demonstrated that CHMs alleviate atherogenesis via mediating pathophysiologic events involved in AS. However, there is deficiency in the summaries regarding antiatherogenic signal pathways regulated by CHMs. In this review, we focus on the signal cascades by which herb medicines and relevant extractives, derivatives, and patents improve proatherogenic processes including endothelium dysfunction, lipid accumulation, and inflammation. We mainly elaborate the CHMs-mediated signaling pathways in endothelial cells, macrophages, and vascular smooth muscle cells of each pathogenic event. Moreover, we briefly describe the other AS-related factors such as thrombosis, autophagy, immune response, and noncoding RNAs and effects of CHMs on them in the way of cascade regulation, which is helpful to further illustrate the molecular mechanisms of AS initiation and progression and discover newly effective agents for AS management.
    Type of Medium: Online Resource
    ISSN: 2314-6133 , 2314-6141
    URL: Article
    DOI: 10.1155/2018/5392375
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2018
    detail.hit.zdb_id: 2698540-8
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  • 2
    Online Resource
    Online Resource
    Hydroxytyrosol Plays Antiatherosclerotic Effects through Regulating Lipid Metabolism via Inhibiting the p38 Signal Pathway
    Hindawi Limited ; 2020
    In:  BioMed Research International Vol. 2020 ( 2020-06-23), p. 1-12
    Details
    In: BioMed Research International, Hindawi Limited, Vol. 2020 ( 2020-06-23), p. 1-12
    Abstract: Purpose . Hydroxytyrosol (HT) processes multiaspect pharmacological properties such as antithrombosis and antidiabetes. The aim of this study was to explore the antistherosclerotic roles and relevant mechanisms of HT. Methods . Male apoE -/- mice were randomly divided into 2 groups: the control group and the HT group (10 mg/kg/day orally). After 16 weeks, blood tissue, heart tissue, and liver tissue were obtained to detect the atherosclerotic lesions, histological analysis, lipid parameters, and inflammation. And the underlying molecular mechanisms of HT were also studied in vivo and in vitro. Results . HT administration significantly reduced the extent of atherosclerotic lesions in the aorta of apoE -/- mice. We found that HT markedly lowered the levels of serum TG, TC, and LDL-C approximately by 17.4% ( p = 0.004 ), 15.2% ( p = 0.003 ), and 17.9% ( p = 0.009 ), respectively, as well as hepatic TG and TC by 15.0% ( p 〈 0.001 ) and 12.3% ( p = 0.003 ), respectively, while inducing a 26.9% ( p = 0.033 ) increase in serum HDL-C. Besides, HT improved hepatic steatosis and lipid deposition. Then, we discovered that HT could regulate the signal flow of AMPK/SREBP2 and increase the expression of ABCA1, apoAI, and SRBI. In addition, HT reduced the levels of serum CRP, TNF- α , IL-1 β , and IL-6 approximately by 23.5% ( p 〈 0.001 ), 27.8% ( p 〈 0.001 ), 18.4% ( p 〈 0.001 ), and 19.1% ( p 〈 0.001 ), respectively, and induced a 1.4-fold increase in IL-10 level ( p = 0.014 ). Further, we found that HT might regulate cholesterol metabolism via decreasing phosphorylation of p38, followed by activation of AMPK and inactivation of NF- κ B, which in turn triggered the blockade of SREBP2/PCSK9 and upregulation of LDLR, apoAI, and ABCA1, finally leading to a reduction of LDL-C and increase of HDL-C in the circulation. Conclusion . Our results provide the first evidence that HT displays antiatherosclerotic actions via mediating lipid metabolism-related pathways through regulating the activities of inflammatory signaling molecules.
    Type of Medium: Online Resource
    ISSN: 2314-6133 , 2314-6141
    URL: Article
    DOI: 10.1155/2020/5036572
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2020
    detail.hit.zdb_id: 2698540-8
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  • 3
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    Table1.DOCX
    Frontiers Media SA ; 2021
    In:  Frontiers in Cell and Developmental Biology Vol. 9 ( 2021-12-17)
    Details
    In: Frontiers in Cell and Developmental Biology, Frontiers Media SA, Vol. 9 ( 2021-12-17)
    Abstract: Anthracyclines, such as doxorubicin (DOX), are among the effective chemotherapeutic drugs for various malignancies. However, their clinical use is limited by irreversible cardiotoxicity. This study sought to determine the role of neuraminidase 1 (NEU1) in DOX-induced cardiomyopathy and the potential cardio-protective effects of NEU1 inhibitor oseltamivir (OSE). Male Sprague–Dawley (SD) rats were randomized into three groups: control, DOX, and DOX + OSE. NEU1 was highly expressed in DOX-treated rat heart tissues compared with the control group, which was suppressed by OSE administration. Rats in the DOX + OSE group showed preserved cardiac function and were protected from DOX-induced cardiomyopathy. The beneficial effects of OSE were associated with the suppression of dynamin-related protein 1 (Drp1)-dependent mitochondrial fission and mitophagy. In detail, the elevated NEU1 in cardiomyocytes triggered by DOX increased the expression of Drp1, which subsequently enhanced mitochondrial fission and PINK1/Parkin pathway-mediated mitophagy, leading to a maladaptive feedback circle towards myocardial apoptosis and cell death. OSE administration selectively inhibited the increased NEU1 in myocardial cells insulted by DOX, followed by reduction of Drp1 expression, inhibition of PINK1 stabilization on mitochondria, and Parkin translocation to mitochondria, thus alleviating excessive mitochondrial fission and mitophagy, alleviating subsequent development of cellular apoptotic process. This work identified NEU1 as a crucial inducer of DOX-induced cardiomyopathy by promoting Drp1-dependent mitochondrial fission and mitophagy, and NEU1 inhibitor showed new indications of cardio-protection against DOX cardiotoxicity.
    Type of Medium: Online Resource
    ISSN: 2296-634X
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fcell.2021.802502
    DOI: 10.3389/fcell.2021.802502.s001
    DOI: 10.3389/fcell.2021.802502.s002
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2737824-X
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  • 4
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    Presentation7.PPTX
    Frontiers Media SA ; 2022
    In:  Frontiers in Cell and Developmental Biology Vol. 9 ( 2022-1-17)
    Details
    In: Frontiers in Cell and Developmental Biology, Frontiers Media SA, Vol. 9 ( 2022-1-17)
    Abstract: Sepsis is a dysregulated systemic inflammatory response that often leads to cardiac dysfunction, which is termed sepsis-induced cardiomyopathy (SIC). Harmine, a natural β -carboline alkaloid compound, has been shown to exert pharmacological effects on several diseases. Here, we investigated whether harmine protected against SIC development and the underlying mechanisms. In vitro , the expression of the M1 phenotype markers iNOS and COX-2 was increased in RAW 264.7 cells stimulated with lipopolysaccharide (LPS), but this effect was reversed by the harmine intervention. Furthermore, LPS-induced increases in the levels of inflammatory cytokines, including IL-1 β , IL-6, TNF- α , iNOS, COX-2, PGE2 and TXB2, generated by macrophages were suppressed when the cells were pretreated with harmine. Meanwhile, our findings showed that harmine administration effectively attenuated inflammation and apoptosis in H9c2 cells in the proinflammatory environment produced by macrophages, as evidenced by reductions in NLRP3 and cleaved caspase 3 levels and the p-NF-κB/NF-κB ratio. The western blot results indicated that the mechanisms underlying harmine-mediated inhibition of M1 polarization might be associated with suppression of STAT1/3, NF-κB and MAPK activation. Furthermore, an LPS injection induced cardiac dysfunction and decreased the survival rate of mice, which were alleviated by harmine treatment, and the relevant mechanism was possibly attributed to a drug-induced attenuation of the inflammatory and apoptotic processes in cardiomyocytes. Collectively, these results implied that harmine treatment protected against SIC by suppressing M1 phenotypic polarization and inflammation in macrophages.
    Type of Medium: Online Resource
    ISSN: 2296-634X
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fcell.2021.792257
    DOI: 10.3389/fcell.2021.792257.s001
    DOI: 10.3389/fcell.2021.792257.s002
    DOI: 10.3389/fcell.2021.792257.s003
    DOI: 10.3389/fcell.2021.792257.s004
    DOI: 10.3389/fcell.2021.792257.s005
    DOI: 10.3389/fcell.2021.792257.s006
    DOI: 10.3389/fcell.2021.792257.s007
    DOI: 10.3389/fcell.2021.792257.s008
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2737824-X
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  • 5
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    Rosuvastatin exerts anti-atherosclerotic effects by improving macrophage-related foam cell formation and polarization conversion via mediating autophagic activities
    Springer Science and Business Media LLC ; 2021
    In:  Journal of Translational Medicine Vol. 19, No. 1 ( 2021-02-10)
    Details
    In: Journal of Translational Medicine, Springer Science and Business Media LLC, Vol. 19, No. 1 ( 2021-02-10)
    Abstract: Atherosclerosis is a chronic vascular disease posing a great threat to public health. We investigated whether rosuvastatin (RVS) enhanced autophagic activities to inhibit lipid accumulation and polarization conversion of macrophages and then attenuate atherosclerotic lesions. Methods All male Apolipoprotein E-deficient (ApoE −/− ) mice were fed high-fat diet supplemented with RVS (10 mg/kg/day) or the same volume of normal saline gavage for 20 weeks. The burden of plaques in mice were determined by histopathological staining. Biochemical kits were used to examine the levels of lipid profiles and inflammatory cytokines. The potential mechanisms by which RVS mediated atherosclerosis were explored by western blot, real-time PCR assay, and immunofluorescence staining in mice and RAW264.7 macrophages. Results Our data showed that RVS treatment reduced plaque areas in the aorta inner surface and the aortic sinus of ApoE −/− mice with high-fat diet. RVS markedly improved lipid profiles and reduced contents of inflammatory cytokines in the circulation. Then, results of Western blot showed that RVS increased the ratio LC3II/I and level of Beclin 1 and decreased the expression of p62 in aortic tissues, which might be attributed to suppression of PI3K/Akt/mTOR pathway, hinting that autophagy cascades were activated by RVS. Moreover, RVS raised the contents of ABCA1, ABCG1, Arg-1, CD206 and reduced iNOS expression of arterial wall, indicating that RVS promoted cholesterol efflux and M2 macrophage polarization. Similarly, we observed that RVS decreased lipids contents and inflammatory factors expressions in RAW264.7 cells stimulated by ox-LDL, accompanied by levels elevation of ABCA1, ABCG1, Arg-1, CD206 and content reduction of iNOS. These anti-atherosclerotic effects of RVS were abolished by 3-methyladenine intervention. Moreover, RVS could reverse the impaired autophagy flux in macrophages insulted by chloroquine. We further found that PI3K inhibitor LY294002 enhanced and agonist 740 Y-P weakened the autophagy-promoting roles of RVS, respectively. Conclusions Our study indicated that RVS exhibits atheroprotective effects involving regulation lipid accumulation and polarization conversion by improving autophagy initiation and development via suppressing PI3K/Akt/mTOR axis and enhancing autophagic flux in macrophages.
    Type of Medium: Online Resource
    ISSN: 1479-5876
    URL: Article
    DOI: 10.1186/s12967-021-02727-3
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2118570-0
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  • 6
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    Beneficial Effects Exerted by Paeonol in the Management of Atherosclerosis
    Hindawi Limited ; 2018
    In:  Oxidative Medicine and Cellular Longevity Vol. 2018 ( 2018-11-07), p. 1-11
    Details
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2018 ( 2018-11-07), p. 1-11
    Abstract: Atherosclerosis, a chronic luminal stenosis disorder occurred in large and medium arteries, is the principle pathological basis of cardiovascular diseases with the highest morbidity and mortality worldwide. In oriental countries, traditional Chinese medicine Cortex Moutan has been widely used for the treatment of atherosclerosis-related illnesses for thousands of years. Paeonol, a bioactive monomer extracted from Cortex Moutan, is an important pharmacological component responsible for the antiatherosclerotic effects. Numerous lines of findings have established that paeonol offers beneficial roles against the initiation and progression of atherosclerotic lesions through inhibiting proatherogenic processes, such as endothelium damage, chronic inflammation, disturbance of lipid metabolism, uncontrolled oxidative stress, excessive growth, and mobilization of vascular smooth muscle cells as well as abnormality of platelet activation. Investigations identifying the atheroprotective effects of paeonol present substantial evidence for potential clinical application of paeonol as a therapeutic agent in atherosclerosis management. In this review, we summarize the antiatherosclerotic actions by which paeonol suppresses atherogenesis and provide newly insights into its atheroprotective mechanisms and the future clinical practice.
    Type of Medium: Online Resource
    ISSN: 1942-0900 , 1942-0994
    URL: Article
    DOI: 10.1155/2018/1098617
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2018
    detail.hit.zdb_id: 2455981-7
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  • 7
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    Empagliflozin alleviates the development of autoimmune myocarditis via inhibiting NF-κB-dependent cardiomyocyte pyroptosis
    Elsevier BV ; 2024
    In:  Biomedicine & Pharmacotherapy Vol. 170 ( 2024-01), p. 115963-
    Details
    In: Biomedicine & Pharmacotherapy, Elsevier BV, Vol. 170 ( 2024-01), p. 115963-
    Type of Medium: Online Resource
    ISSN: 0753-3322
    URL: Article
    DOI: 10.1016/j.biopha.2023.115963
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2024
    detail.hit.zdb_id: 1501510-5
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  • 8
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    A new Mfn-2 related synthetic peptide promotes vascular smooth muscle cell apoptosis via regulating the mitochondrial apoptotic pathway by inhibiting Akt signaling
    Springer Science and Business Media LLC ; 2021
    In:  Journal of Translational Medicine Vol. 19, No. 1 ( 2021-12)
    Details
    In: Journal of Translational Medicine, Springer Science and Business Media LLC, Vol. 19, No. 1 ( 2021-12)
    Abstract: Restenosis after angioplasty is a major challenge for the treatment of coronary artery diseases. Facilitation of vascular smooth muscle cell (VSMC) apoptosis may be an attractive approach to decrease the incidence of restenosis. We synthesized a 16-amino acid mitofusin-2 (Mfn-2) gene related peptide (MRSP) based on the sequence of the p21 ras signature motif, the smallest functional sequence of the Mfn-2 gene with proapoptotic properties in VSMC. We investigated whether MRSP enhanced apoptotic activities to inhibit VSMC accumulation and neointimal hyperplasia in rats with carotid balloon injury. Methods VSMCs were treated with different concentrations of MRSP, the PI3K agonist 740 Y-P and the inhibitor LY294002. Cell apoptosis and related pathway molecules were assessed. MRSP was also given to rats with carotid artery balloon injury. Neointimal hyperplasia and cell apoptotic pathways were detected. Results In vitro experiments revealed that MRSP treatment significantly increased VSMC apoptosis and induced increases in procaspase-9 cleavage, caspase-3 activation, cytochrome c release from mitochondria to the cytoplasm and the Bax/Bcl-2 ratio but not caspase-8 expression, indicating that the mitochondrial apoptotic cascade was activated by MRSP, which might be attributed to suppression of the PI3K/Akt signaling pathway. We further found that the PI3K agonist 740 Y-P prevented and that the inhibitor LY294002 strengthened the proapoptotic effects of MRSP. MRSP strongly inhibited neointimal hyperplasia and VSMC accumulation, but increased VSMC apoptosis in the vascular wall after balloon injury. Moreover, MRSP substantially enhanced Bax and cleaved caspase-3 expression and decreased Bcl-2 levels in intima, accompanied by decreased levels of phosphorylated Akt and PI3K in vivo. Conclusions Taken together, the present study showed that MRSP treatment results in a strong proapoptotic effect by activating the mitochondrial apoptotic cascade through suppression of the PI3K/Akt pathway.
    Type of Medium: Online Resource
    ISSN: 1479-5876
    URL: Article
    DOI: 10.1186/s12967-021-03064-1
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2118570-0
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  • 9
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    Shexiang Baoxin Pill Alleviates the Atherosclerotic Lesions in Mice via Improving Inflammation Response and Inhibiting Lipid Accumulation in the Arterial Wall
    Hindawi Limited ; 2019
    In:  Mediators of Inflammation Vol. 2019 ( 2019-07-11), p. 1-13
    Details
    In: Mediators of Inflammation, Hindawi Limited, Vol. 2019 ( 2019-07-11), p. 1-13
    Abstract: Epidemiological studies have demonstrated that cardiovascular diseases (CVDs) are the leading cause of death in the world. Atherosclerosis, a kind of chronic vascular disorder related to multiple pathogenic processes, has been reported to be an underlying cause of CVDs. Shexiang Baoxin Pill (SBP) is a traditional Chinese medicine formulation and has been broadly used for the treatment of CVDs in East Asia. However, whether SBP affects the development of atherosclerosis is poorly understood. The aim of this study was to investigate the antiatherosclerotic roles and relevant mechanisms of SBP in apolipoprotein E knockout mice. Our results showed that SBP treatment markedly decreased the size of atherosclerotic plaques of the entire aorta and the aortic sinus. Biochemical analyses indicated that SBP gavage improved oxidative stress in vivo, as seen by the level elevation of SOD, CAT, and GSH and the level reduction of MDA, H 2 O 2 , and MPO. Moreover, the concentration of MCP-1, IFN- γ , and IL-17A was reduced, and the content of IL-10 and TGF- β 1 was increased in the serum from SBP-treated mice. We discovered that the expression levels of inflammatory factors including VCAM-1, ICAM-1, IL-6, and IL-2 in the vascular wall of the SBP group were also decreased in comparison with those of the normal saline group. Moreover, we found that SBP alleviated the activation of inflammation-related pathways in the aorta tissue, as seen by the level elevation of Mfn2 and reduced phosphorylation of p38, JNK, and NF- κ B. Furthermore, western blot showed that SBP administration reduced the level of SR-A and LOX-1 and elevated the content of LXR α , ABCA1, and ABCG1 in the arterial wall, indicating that SBP was capable of alleviating lipid influx and facilitating lipid efflux. In conclusion, our data suggested that SBP exerted antiatherosclerotic effects via improving inflammation response and inhibiting lipid accumulation.
    Type of Medium: Online Resource
    ISSN: 0962-9351 , 1466-1861
    URL: Article
    DOI: 10.1155/2019/6710759
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2019
    detail.hit.zdb_id: 2008065-7
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  • 10
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    The atheroprotective roles of heart-protecting musk pills against atherosclerosis development in apolipoprotein E-deficient mice
    AME Publishing Company ; 2019
    In:  Annals of Translational Medicine Vol. 7, No. 23 ( 2019-12), p. 714-714
    Details
    In: Annals of Translational Medicine, AME Publishing Company, Vol. 7, No. 23 ( 2019-12), p. 714-714
    Type of Medium: Online Resource
    ISSN: 2305-5839 , 2305-5847
    URL: Journal
    URL: Article
    DOI: 10.21037/atm
    DOI: 10.21037/atm.2019.12.22
    Language: Unknown
    Publisher: AME Publishing Company
    Publication Date: 2019
    detail.hit.zdb_id: 2893931-1
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